MHCs are slutty- a single MHC can bind to multiple Ag peptide sequences Polygenic- use both mom and

dad alleles instead of knocking one out like in Ab production- results in high diversity-which is important MHC1- intracellular bad protein meets proteasome and is degraded, sent to RER and loaded onto MHC1 then sent to golgi MHC2s are corked until they reach the phagolysosome then bind with Ag-prevents unwanted binding

Abs-Constant region of Ab determine class

Complement receptors (CR) along with FC receptors are on the surface of Phagocytes, and B cells (CR2) Classical- each C1 complex must bind by its C1q head to at least 2 Fc sites for a stable C1-Ab-Ag interaction. Bind immune complexes to cells, helps in extravasation, opsonation, induces degranulation of mast cells (inflam) RBCs can use comp to grab bad guys and send em to the liver Cleaved portions can act as chemotactic factors Lambda and kappa are both light chains Either of the lambda Vs can combine with any of the functional J/C combinations Any of the kappa Vs can join with any of the Js. The heavy chain or mew has a V that can join with any D and together can combine with any of the Js. NO DS ON LIGHT CHAIN! The rearranging (which produces the variable regions on Ab) happens before transcription. RNA splicing will then remove any unwanted remaining nucleic acid. Surrogate light chain is made after heavy, contains just constants Prevents H chain from degrading Lambda light chain is made last Rearrangement leads to 2.6e6 possible variations For class switching, Th is needed, which means antigen peptide presentation. If not, IgM is just made matching a shape. No memory either, so all PRIMARY response IL-4 is a cytokine released by Th2 and helps switch C regions-DF DNA coding for light & heavy chains are on separate chromosomes
DONT FORGET TO TALK ABOUT ALLELIC EXCLUSION!!!!!

T helper cells once stimulated release IL-2 which is a TCGF

Th2 inhibits Th1 growth because its not needed for an extracellular response Tcells use a very selective system with less mistakes than Bcells Proliferation occurs on a CD4 or CD8 Tcell once its TCR binds to its corresponding antigen on MHC2 and 1 respectively. (IL-2) Blood Ab is always IgM bc it reacts to sugars on RBCs not protein. For a class switch, need Th and therefore a peptide chain GF & DF secreted by Th2 cells only signal Bcells that have been activated by the same antigen ready to be activated CTLs and B cells have recently made GF and DF receptors on their membranes

No Ab can have multiple specificities-dangerous MDGAE!!! D is a signaling molecule Once Ab-Ag complex is made, Fc portion changes configuration so a phag can bind to it---opsonization

Innate CMI NK
Activated Phags (TLRs)

Responses Humoral Alt. comp interferon

Danger Will Robinson

Unlike the SNS model, the danger hypothesis relies on damaged cells as signaling molecules rather than immune cells distinguishing between self and non self molecules. There is a difference between a normal cell dying quietly (apoptosis) and one being murdered. The murdered cell leaves alarm signals telling the body than an immune response is needed The alarm signals are just intracellular components of the dead cell which the immune system has never came into contact with. Called DAMPs The theory negates TLRs because they are preprogrammed with knowledge of bag guy composition The fact that the immune system may reject transplants supports this theory, and also why malignant tumors are not attacked and destroyed Matzinger also believes that Treg cells are not responsible for shutting down immune responses against self and commensal bacteria And just in case Im having a brain aneurism tomorrow, in which case im screwed either way, but specificity, memory, sns

Random stuff
All nave B&T cells will apoptose if its corresponding Ag is never found ONLY 1 SPECIFICITY PER Ab, WAY TOO DANGEROUS TO HAVE MULTIPLE SPECIFICITIES Toll Like Receptors are on most phagocytes and recognize highly conserved regions on pathogens They are Pattern Recognition Receptors that distinguish SNS via Pathogen Associated Molecular Patterns LPS on gram neg bacteria has a high affinity to TLR-4 and is a great stimulator of innate immunity Bad guys cannot mutate structures like LPS to avoid detection because it is extremely important for the vitality of the micro-organism Once stimulated, signal transduction that leads to expression of genes that induce inflammation and increase antigen presentation